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To optimize the field emission behavior of the ZnO nanorods, postthermal annealing in different ambience was conducted. The field emission properties of the ZnO nanorods are considerably improved after annealing in oxygen and getting worse when annealing in air or ammonia. Photoluminescence and Raman spectroscopy were employed to elucidate the reason for such a significant improvement of the field emission when annealing in oxygen. Those detailed analyses suggested that oxygen annealing can reduce the oxygen vacancy concentration, improve the crystal quality, lower the work function, and increase the conductivity of the ZnO nanorods. Our work is important for applications of ZnO nanorods as a promising candidate in flat panel displays and high brightness electron sources.

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The 1:1 adduct of arginine with 2,5-dihydroxybenzoic acid (DHB) has been studied in the gas phase and in the solid state. Experimentally, the ionization energy (IE) of the 1:1 cluster was determined by wavelength-dependent laser ionization of clusters formed by seeding DHB and arginine into a supersonic jet expansion. Ionization laser power studies performed at several discrete wavelengths established the upper and lower limits for the 1:1 cluster IE and dissociation energy. Subsequent one-color scanned-wavelength laser ionization studies allowed an experimental establishment of the 1:1 cluster IE of 7.193 eV. A combination of molecular dynamics/simulated annealing calculations on the 1:1 cluster followed by density functional theory geometry optimizations using reasonably large basis sets yielded 15 distinct minima on the potential energy surface, all within 5.2 kcal/mol in energy at the B3LYP/6-311++G(2df,2p)//B3LYP/6-31+G** level. The Boltzmann-averaged IE at the same level is 7.11−7.14 eV, in excellent agreement with experiment. Cocrystals of arginine and DHB have been grown, and the crystal structure has been solved. The dominant intermolecular interaction in the cocrystal is a double hydrogen bond (salt bridge) between the guanidinium group of arginine and the (deprotonated) carboxylate group of DHB. This is exactly the same interaction that is found in the lowest-energy structure of the gas-phase 1:1 adduct. The electronic structure of the solid-state cocrystal has been modeled using a cluster approach.

Zinc finger protein 139(ZNF139), a member of zinc finger protein family, is a transcription factor. Our previous research showed ZNF139 was overexpressed in gastric cancer cells. The purpose of present study is to explore impact and mechanism of ZNF139 on metastasis by regulating invasive ability of gastric cancer cells.Quantitative RT-PCR(QRT-PCR) and Western blot were applied for detection of ZNF139 expression in gastric cancer tissues, adjacent cancer tissues, metastatic lymph nodes, gastric cancer cell lines SGC7901 and BGC823 and gastric epithelial cell line GES-1; siRNA specific to ZNF139 was synthesized and then transfected into gastric cancer cell line BGC823; wound healing assay and Transwell assay were used to observe impact of ZNF139-siRNA after being transfected into BGC823 on its invasion and migration; changes in expression of invasion and migration-related genes MMP-2, MMP-9, ICAM-1 and TIMP1 were detected before and after transfection. Gelatin zymogrphy assay were applied to determine the MMP activities. Statistical analysis was based on the SPSS11.5 software.Expression of ZNF139 in gastric adenocarcinoma tissues and cells was significantly higher than the expression in the adjacent cancer tissues, but lower than the expression in the metastatic lymph nodes; ZNF139 expression was present in gastric cancer cell lines, and the expression level was higher than that in normal gastric epithelial cells lines. ZNF139-siRNA significantly inhibited the invasion and migration activity of gastric cancer cell line BGC823. 48h after ZNF139-siRNA was transfected into gastric cancer cell line BGC823, expression and activity of invasion-related genes MMP-2, MMP-9, ICAM-1 mRNA and protein were significantly inhibited, while expressions of TIMP-1 mRNA and protein were significantly increased. At the same time, the gelatinase activities of MMP2 and MMP9 were decreased by ZNF139 interference.ZNF139 was overexpressed in gastric cancer cells, and the expression was further enhanced in the metastasis process. Knocking down ZNF139 expression in gastric cancer cells could effectively reduce gastric cancer cell invasion and migration ability, and this process might play a role by regulating MMP-TIMP balance. Key words: gastric cancer, zinc finger protein 139(ZNF139), migration, invasion, RNA interference technologyGastric cancer is currently the second leading cancer killer in the world. High incidence of gastric cancer exists in east Asia, which is also the leading cause of death in malignant tumor in China. Gastric cancer has strong ability for proliferation, invasion and metastasis, which is one of the important factors that lead to poor prognosis. A variety of genes in tumor cells and their expression products play an important role in the invasion and metastasis process of gastric cancer [1][2][3][4]. It has been a hotspot to treat gastric cancer by inhibiting invasion and migration capability of gastric cancer cells, and the study has made some achievements [5][6][7]. But there has yet not been a breakthrough in the...

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